OBJECTIVES: Patients with Helicobacter pylori (HP) infection have been reported to have in addition to duodenitis architectural changes of the duodenal bulb mucosa including villous atrophy and crypt hyperplasia. We here for the first time present two cases of HP-infected adult patients with a crypt hyperplastic enteropathy also in the distal duodenum mimicking celiac disease (CD). METHODS: We evaluated separately the morphology of the anatomical bulb and distal duodenal mucosa using validated quantitative morphometric tools, i.e., the villous height (VH) and crypt depth (CrD) and their ratios. The fresh frozen samples were evaluated for the presence of the CD-specific transglutaminase 2-targeted subepithelial IgA deposits. RESULTS: Both patients had celiac-type crypt hyperplastic mucosal injury in the distal part of the duodenum in the absence of serum autoantibodies and subepithelial IgA deposits. After two years follow-up, having still a normal gluten-containing diet, none of the patients developed CD. Moreover, in the patient re-biopsied two years later, the CD-type enteropathy had healed after HP eradication. CONCLUSIONS: Prospective studies on HP-infected patients are needed in order to confirm our findings.
OBJECTIVES:Patients with Helicobacter pylori (HP) infection have been reported to have in addition to duodenitis architectural changes of the duodenal bulb mucosa including villous atrophy and crypt hyperplasia. We here for the first time present two cases of HP-infected adultpatients with a crypt hyperplastic enteropathy also in the distal duodenum mimicking celiac disease (CD). METHODS: We evaluated separately the morphology of the anatomical bulb and distal duodenal mucosa using validated quantitative morphometric tools, i.e., the villous height (VH) and crypt depth (CrD) and their ratios. The fresh frozen samples were evaluated for the presence of the CD-specific transglutaminase 2-targeted subepithelial IgA deposits. RESULTS: Both patients had celiac-type crypt hyperplastic mucosal injury in the distal part of the duodenum in the absence of serum autoantibodies and subepithelial IgA deposits. After two years follow-up, having still a normal gluten-containing diet, none of the patients developed CD. Moreover, in the patient re-biopsied two years later, the CD-type enteropathy had healed after HP eradication. CONCLUSIONS: Prospective studies on HP-infectedpatients are needed in order to confirm our findings.